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Prenatal Choline Supplementation Improves Glucose Tolerance and Reduces Liver Fat Accumulation in Mouse Offspring

Isma'il Kadam1,2, Steven E Trasino3, Hunter Korsmo1,2

  • 1PhD Program in Biochemistry, Graduate Center of the City University of New York, New York, NY 10016, USA.

Nutrients
|May 11, 2024
PubMed

Insights

Prenatal and postnatal alcohol exposure (AE) can harm offspring metabolism. Maternal choline supplementation (CS) partially prevented alcohol-induced liver fat accumulation and improved glucose tolerance in male mice.

Area of Science:

  • Metabolic health
  • Developmental toxicology
  • Nutritional neuroscience

Background:

  • Prenatal alcohol exposure (AE) is known to impact cognitive development.
  • The effects of prenatal AE on offspring metabolic health and the exacerbation by postnatal AE remain unclear.
  • Choline, a vital nutrient, has shown promise in mitigating AE-induced cognitive deficits.

Purpose of the Study:

  • To investigate the protective effects of maternal choline supplementation (CS) against metabolic disturbances in offspring exposed to both prenatal and postnatal alcohol (AE/AE).
  • To assess the impact of AE/AE on hepatic lipid accumulation, glucose tolerance, and related gene expression.
  • To determine if prenatal CS can ameliorate AE/AE-induced metabolic impairments.

Main Methods:

  • C57BL/6J mice underwent maternal dietary ethanol exposure from embryonic day 9.5 to 17.5, with or without choline supplementation.
  • Offspring were exposed to ethanol postnatally for four weeks.
  • Hepatic triglyceride levels, glucose tolerance, and expression of key metabolic genes (Ppara, Ldlr) were analyzed.

Main Results:

  • Alcohol-exposed/alcohol-exposed (AE/AE) male offspring exhibited increased hepatic triglyceride accumulation, which was normalized by prenatal choline supplementation (CS).
  • Prenatal CS also improved glucose tolerance in AE/AE offspring compared to unsupplemented AE/AE animals.
  • AE/AE suppressed hepatic Ppara and Ldlr gene expression in males, but these changes were not reversed by prenatal CS.

Conclusions:

  • Combined prenatal and postnatal alcohol exposure (AE/AE) increases the risk of hepatic steatosis in male offspring.
  • Maternal choline supplementation offers partial protection against AE/AE-induced metabolic dysfunction, particularly concerning liver fat accumulation and glucose tolerance.
  • Further research is needed to understand the mechanisms underlying the partial efficacy of prenatal CS on AE/AE-induced metabolic changes.

Keywords:
cholineglucose toleranceprenatal alcohol exposuresteatosis

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